ArticleFrontiers in immunology2026
Loss of Akt3 enhances antiviral immunity while disrupting corneal homeostasis during ocular HSV-1 infection.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Background: Akt1 and Akt2 isoforms reveal distinct immune-regulatory roles in HSV-1 pathogenesis. Akt3 is a developmentally important protein, and mutations in Akt3 gene are associated with a wide spectrum of developmental disorders, including extreme megalencephaly; however, its role in corneal homeostasis and pathologies remains poorly understood. Here we investigated the role of Akt3 in HSV-1 infection. Methods: Results: In this study, we report the significance of the Akt3 isoform in HSV-1 viral pathogenesis. Loss of Akt3 at baseline results in spontaneous corneal opacity, suggesting it is a critical regulator of ocular homeostasis. Despite this baseline compromise, Akt3 deficient mice appear to be better protected against HSV-1 infection, showing lower titers and better survivability. Loss of Akt3 plays a unique role in regulating type 1 interferon production necessary for combating viral infection, along with demonstrating significantly higher serum neutralizing capacity compared to WT controls. Conclusion: Akt3 deficiency reconfigures the innate-adaptive interface acting as a negative modulator of the antiviral response during HSV-1 infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.